title: Activated inflammatory cells participate in thrombus size through tissue factor and plasminogen activator inhibitor-1 in acute coronary syndrome: Immunohistochemical analysis.
abstract: BACKGROUND
  Recent studies have suggested that circulating inflammatory cells augment the growth of thrombus in acute coronary syndrome (ACS). We therefore immunohistochemically analyzed thrombi in aspirates obtained from patients immediately after the onset of ACS.
  
  
  METHODS
  Two hundred twenty samples were studied. Total thrombus area, white thrombus area, and red thrombus area were measured. As antibodies in immunohistochemical staining, myeloperoxidase (MPO), CD66b, CD68, p-selectin, tissue factor (TF) and PAI-1 were employed respectively.
  
  
  RESULTS
  The ratios of areas of red and white thrombi correlated with whole sample areas of enlarged thrombi (r = 0.48, p < 0.001). The immunohistochemical findings revealed granulocytes and macrophages aggregated around p-selectin-positive platelets that shared the boundary between white and red thrombi, a region where MPO and CD66b expression was abundant in neutrophils. The ratios (%) of MPO- and CD66b-positive cells significantly correlated with whole sample areas (r = 0.50; p < 0.001 and r = 0.49; p < 0.001, respectively). Neutrophils and macrophages within thrombi were positive for TF and PAI-1. Along the boundary between red and white thrombi, TF and PAI-1 positivity coincided with MPO-, CD66b- and CD68-positive cells. The ratios of cells positive for both TF and PAI-1 in this area significantly correlated with the whole sample area (r = 0.43, p < 0.001 and r = 0.60, p < 0.001, respectively).
  
  
  CONCLUSIONS
  These results suggested that enhanced activation of peripheral neutrophils together with increased TF and PAI-1 expression might comprise a considerable portion of thrombus enlargement.
authors.affiliation: Division of Cardiology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan. VZF07217@nifty.com
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Sakai
authors.forename: Shin
authors.initials: S
authors.lastname: Inoue
authors.forename: Masatoshi
authors.initials: M
authors.lastname: Takei
authors.forename: Genyo
authors.initials: G
authors.lastname: Ogawa
authors.forename: Yuji
authors.initials: Y
authors.lastname: Hamazaki
authors.forename: Hidekazu
authors.initials: H
authors.lastname: Ota
authors.forename: Youichi
authors.initials: Y
authors.lastname: Koboyashi
mesh_terms: D054058:Acute Coronary Syndrome / Q000378:metabolism* / Q000473:pathology*; D000208:Acute Disease; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D018836:Inflammation Mediators / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000378:metabolism*; D013925:Thromboplastin / Q000378:metabolism*; D013927:Thrombosis / Q000378:metabolism / Q000473:pathology
chemical_list: D018836:Inflammation Mediators; D017395:Plasminogen Activator Inhibitor 1; D013925:Thromboplastin